The NTRK3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, designed for functional loss-of-function studies of the NTRK3 gene. This product offers a heterogeneous pool of edited cells, enabling robust investigation of NTRK3-dependent signaling without the influence of clonal selection artifacts. The targeted disruption of NTRK3 ablates the expression of full-length TrkC receptor tyrosine kinase, providing a genetically defined model to dissect the role of this neurotrophin receptor in lymphocyte biology and beyond.
Raji is a widely utilized human Burkitt??s lymphoma B lymphocyte line that is Epstein-Barr virus (EBV) positive and endogenously expresses B-cell lineage markers CD19, CD20, and CD22. This suspension cell line serves as a canonical model for B-cell malignancies and immune cell signaling, offering a physiologically relevant background for studying the intersection of oncogenic and neurotrophin pathways in hematopoietic cells.
NTRK3 encodes the TrkC receptor, which is specifically activated by the neurotrophin NT-3, and to a lesser extent by BDNF and NT-4/5. Upon ligand-induced dimerization and autophosphorylation, TrkC recruits adaptor proteins including GRB2 and SHC1, triggering downstream cascades such as the RAS?CRAF?CMEK?CERK (MAPK1/3) pathway and the PI3K?CAKT1?CmTOR axis. Additionally, PLC??1-mediated signaling generates second messengers IP3 and DAG, mobilizing calcium and activating PKC. TrkC also interacts with the p75NTR co-receptor and modulators like SHP2 (PTPN11), FRS2, and sortilin (SORT1) to fine-tune cellular responses. In non-neuronal tissues, NTRK3 signaling influences proliferation, survival, and apoptosis, while oncogenic fusions drive constitutive activation in multiple cancer types.
By disrupting NTRK3 in the Raji B-cell background, researchers can interrogate the role of NT-3/TrkC signaling in lymphocyte proliferation, survival, and transformation. Although NTRK3 is not classically associated with B-cell lymphomas, emerging evidence suggests that neurotrophin receptors may modulate immune cell functions and chemosensitivity. This knockout model enables dissection of TrkC-dependent signals in a cell line that already harbors MYC deregulation, providing a platform to study cooperative oncogenic pathways and evaluate the specificity of TRK inhibitors in a hematologic context.
Typical applications include functional rescue experiments, phospho-signaling analysis using flow cytometry or immunoblotting for phospho-ERK1/2 and phospho-AKT1, and proliferation and apoptosis assays in the presence of NT-3 or TRK inhibitors such as larotrectinib. The polyclonal population also serves as an ideal control for RNA-seq studies to identify NTRK3-dependent transcriptional programs in B cells. Furthermore, this model facilitates high-throughput screening for compounds that selectively target NTRK3-driven signaling versus other kinases. For technical specifications and ordering details, please contact Ascent Research.
